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Tag: glutamate
Fasoracetam Nootropics Racetams Reviews
Fasoracetam: How This Nootropic May Help You Focus Better
Post author By Staff
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Originally known as NS-105, Fasoracetam is one of the newest nootropics on the market. Besides being the latest racetam to be discovered, it has some unique properties unlike any other racetam on the market. Let's find out what makes this substance a truly unique nootropic, and why you should (or should not) try it.
One of the primary effects of Fasoracetam is the modulation of metabotropic glutamate receptors II and III (mGluR).[1] mGlu receptors have been shown to be involved in synaptic plasticity and neuroprotection. In addition, LY354740, am mGlu2/3 agonist, has been shown to be effective in generalized anxiety disorder.[2]
Fasoracetam is also the only racetam that significantly enhances cAMP formation[3] and that has been shown to be potentially effective in individuals with glutamatergic gene variants that are suffering from ADHD[4]. A Phase III clinical trial is near completion, but the drug is not currently listed as an ADHD treatment by the FDA.
Fasoracetam has also shown to have antidepressant effects[5] and to counteract learned helplessness, an avoidance behavior typically associated with depression. Fasoracetam, however, does not act on serotonin and other monoamines, and researchers think the antidepressant effect may stem from its ability to upregulate GABA-B receptors.[6]
Generally speaking, Fasoracetam has shown to be more effective with chronic use, and, in the ADHD study, most benefits were felt at week five onward.[7]
In rat studies, fasoracetam restores the function of key receptors, glutamate mGluR II and III[8]. It also upregulates GABA-B receptors through receptor antagonism[9], a fact which may be related to its ability to reverse phenibut tolerance (which is one of the few supplements reported to relieve anhedonic depression). The GABA-B receptor is very important and has been found to play a role in cognition[10], anxiety and mood.
Alcohol, a very disinhibiting and fog-inducing compound (with pleasurable effects similar to phenibut) is thought to achieve its activity by activating GABA-B and A receptors (as well as dopamine). However, because it downregulates these receptors, prolonged use may cause anxiety and cognitive disruptions. Phenibut binds in a similar fashion to GABA-B.
Because of its relatively narrow range of receptor targets, fasoracetam does not feel like a classic stimulant nor does it alter one's feeling of wakefulness. It lacks clinical dopamine activity but remarkably still managed to address ADHD symptoms, according to the study. It is not clear how fasoracetam has such a specific utility in treating ADHD, more research on other neurotransmitters may be turned up in coming years, but judging on present evidence, it seems that Fasoracetam could reduce ADHD symptoms by modulating glutamatergic receptors.
That being said, the FDA does not list Fasoracetam as an ADHD medication and it should not be used as such. Only a professional can prescribe medications for ADHD and you should not self medicate.
Although it is a newer supplement without much of a user-base, it does appear to be well-tolerated even in large doses or extended periods. Among college students, it may soon become a mainstay, alongside other trusted nootropics such as Bacopa, Modafinil, and Noopept.
In addition to the findings surrounding glutamate and ADHD, rat studies have also revealed fasoracetam to have profound cholinergic activity. Many common nootropics work by controlling acetylcholine, including several drugs used in the treatment of Alzheimer's.
It increases the uptake of choline at sites in key brain regions involved in intelligence and mood, the hippocampus and cerebral cortex. This, in turn, results in increased production and release of acetylcholine.[11]
This, similarly to what has been commonly reported with piracetam, may explain a need for choline supplementation in the case of symptoms such as low mood, headache or brain-fog.
Although I personally have only ever tried piracetam and aniracetam (and found, despite a slight cognitive boost, that they both caused a slightly lowered mood, with piracetam being more stimulating and anxiety-prone while aniracetam was calm and relaxing), I haven't read any complaints of fasoracetam and depression (on the contrary it appears to be a robust antidepressant nootropic, similar to tianeptine). This is remarkable because excessive acetylcholine production is typically associated with low mood and depression. Even with something as mild as bacopa, reports of moodiness are easy to pin down.
Since all three of the mentioned racetams seem to operate through a shared mechanism of acetylcholine, it's not clear how fasoracetam achieves a similar cognitive boost without side effects on mood. Perhaps it has been less trialed and as more users sample it, more negative reports will pour in. This seems unlikely, however, given multiple reports of antidepressant effects, and at higher doses, near euphoria.
Fasoracetam and coluracetam are interesting racetams with multiple mechanisms of action compared to piracetam. Although they both share a cholinergic effect, the former modulates mGlu receptors (as well as GABA-B receptors) while the latter interacts with a process named high-affinity choline uptake. This may explain their calm, clear effects when compared with the more bland effects of piracetam.
Of the eight known metabotropic glutamate receptors, only one and five are believed to increase NMDA receptor activity and neural excitation (these two are postsynaptic). The other six receptors all function to lower NMDA (and are presynaptic), lessen excitation and thus reduce potential neurotoxicity.
By slightly lowering glutamate activity and at the same time boosting GABA-B levels, fasoracetam offers a collected state of mind compared to piracetam's more scattered one. Normal tasks would flow much easier, and performance would be improved without adverse effect.
While OCD and more recently schizophrenia have been described as hyperglutamatergic, ADHD has always been thought of as a condition of low glutamate.[12]
However, fasoracetam may very well regulate the metabotropic receptors in both directions and benefit everyone equally (restoring both high and low activity of the receptors to normal).
It is not clear how to explain the remarkable improvements reported in samples of both schizophrenia and ADHD. An explanation may be the selectiveness for the presynaptic mGluRs (mGluR1 and mGluR5) coupled with the fact that these receptors both elevate cAMP and lower NMDA activity. Levels of these receptors in the body are both altered in schizophrenia (so fasoracetam would produce two favorable alterations for the schizophrenic patient).
Despite all this fine talk about schizophrenia and glutamate, most of the reports surrounding fasoracetam are concerned with ADHD symptoms, specifically motivation and focus. It is not widely known for its use as psychiatric medicine, and it may be considered by ADHD patients who have not responded well to conventional treatments. Again, it is not approved by the FDA as an ADHD treatment, and we are not suggesting people suffering from that disease to use it without a medical prescription.
As stated above fasoracetam appears to have GABA-B antagonistic properties[13], and it may upregulate these receptors and thus diminish the tolerance to GABA-B agonists like Phenibut, Baclofen, and Alcohol, and may even act as an "antidote" to a Phenibut overdose.
Before many of the newer designer supplements hit the market and much was known about fasoracetam, Noopept was one of the more recommended supplements for alcoholics to recover cognitive capacities. But in light of this newer evidence, fasoracetam may address the issue more directly. Because of its activity here, fasoracetam may eventually find use in treating age-related memory decline, dementia, and even depression. For now, the research and hype seem to surround the potential treatment of ADHD symptoms.
Dosage and half-life
No dependence potential was noted in the rhesus monkey over the course of four weeks.[14] However. users cannot be completely absolved of concern, due to interspecies differences and the possibility of an only mildly addictive substance requiring an exceptionally long habituation period.
If its use is not completely discouraged in elderly patients, significant caution and close monitoring are recommended. Its metabolism and clearance depend heavily on the kidneys and at least one studied has reported significant accumulation in the elderly (whose renal function is typically compromised).[15]
It is typically taken at 10mg twice daily, but it is probably best to start with 5 mg and taper up. Even though the dosage is very low, bitterness is still a problem and the use of capsules or parachuting is recommended.
Although some work their way up to 30 mg in one dose, this may not be the most effective strategy (due to a short half-life of the compound) and this pattern of use is more likely to be helped along by a large meal. A potent nootropic with a half-life of around 90 minutes, taking it even once a day may be enough for active levels to build up in your system, but tolerance will be close behind.
You can buy Fasoracetam capsules and powder at Nootropics Depot. Fasoracetam is not approved by the FDA as an ADHD treatment.
Reviewer 8.8
» Buy it
1, 3, 8. ↑ Involvement of metabotropic glutamate receptors in Gi- and Gs-dependent modulation of adenylate cyclase activity induced by a novel cognition enhancer NS-105 in rat brain. (1997)
2. ↑ Efficacy and tolerability of an mGlu2/3 agonist in the treatment of generalized anxiety disorder (2008)
4, 7. ↑ Exploratory Dose-Escalation Study of NFC-1 in ADHD Adolescents With Glutamatergic Gene Network Variants
5, 6. ↑ Effect of a novel cognition enhancer NS-105 on learned helplessness in rats: possible involvement of GABA(B) receptor up-regulation after repeated treatment. (1997)
9, 11, 13. ↑ Involvement of cholinergic and GABAergic systems in the reversal of memory disruption by NS-105, a cognition enhancer. (1999)
10. ↑ Role of GABA(B) receptors in learning and memory and neurological disorders. (2016)
12. ↑ On the role of cortical glutamate in obsessive-compulsive disorder and attention-deficit hyperactivity disorder, two phenomenologically antithetical conditions. (2000)
14. ↑ Study on the dependence potential of (+)-5-oxo-D-prolinepiperidinamide monohydrate (NS-105) in rhesus monkeys and rats. (1998)
15. ↑ Comparison of pharmacokinetics of NS-105, a novel agent for cerebrovascular disease, in elderly and young subjects. (1999)
Tags acetylcholine, ADHD, antidepressant, anxiety, depression, fasoracetam, glutamate, memory, nootropics, racetams
Nootropics Tianeptine
Tianeptine: A Nootropic Antidepressant?
Post author By Micah Jahns
3 Comments on Tianeptine: A Nootropic Antidepressant?
Tianeptine is an antidepressant, neuroprotective, and anxiolytic drug developed by French researchers Antoine Deslandes and Michael Spedding in the 1980s. It is currently marketed under the trade names Stablon and Coaxil in some European, Asian, and South American countries.
In the United States, Tianeptine is not FDA approved, mainly due to a lack of interest in the drug within the American pharmaceutical sphere. Although it is typically used in a clinical setting to treat depression and related illnesses, it has recently gained favor among nootropic users for its mood and cognition-boosting capabilities. It remains an unscheduled substance in the US, and can be purchased online via several nootropic vendors.
Relation to Other Antidepressants
In strict terms of chemical structure, Tianeptine is a tricyclic antidepressant (TCA) and is structurally similar to many prescription TCAs, such as amitriptyline and doxepin. However, Tianeptine's mechanism of action varies drastically from classical TCAs
Most TCAs work as serotonin-norepinephrine reuptake inhibitors (SNRIs), increasing the levels of extracellular serotonin and norepinephrine. Tianeptine, however, has been found to enhance the reuptake of serotonin, which would consequently decrease serotonin levels in subjects. In addition, Tianeptine does not possess affinity for most neurotransmitter receptors, meaning it has little to no direct impact on norepinephrine and dopamine.[1]
These findings have led some researchers to question what is known as the monoamine hypothesis of depression, which has prevailed in medical circles for around half a century. Monoamines are a group of neurotransmitters that includes dopamine, serotonin, and norepinephrine, the three of which are linked to motivation and mood. The monoamine hypothesis of depression posits that depression is caused by a shortage of monoamine neurotransmitters in the brain.
Most classical antidepressants, (SSRIs, SNRIs, MAOIs, etc.) seek to restore balance to monoamine levels in the brain, thus alleviating symptoms of depression.[2] The fact that Tianeptine has little effect on monoamine levels, yet still alleviates symptoms of depression, has fortified the evidence that depression is much more complex than just an imbalance of monoamine neurotransmitters.
So, then, how exactly does Tianeptine mitigate the symptoms of depression? Some researchers have hypothesized that depression is directly linked to lowered neuroplasticity (the ability of the brain to adapt to new stimuli) and that an increase in neuroplasticity in the human brain will contribute to reducing symptoms of depression. Studies conducted on Tianeptine's action certainly support this idea.
Essentially, Tianeptine modulates the action of glutamate, the main excitatory neurotransmitter in the brain. Stressful situations tend to augment glutamate's pathways, either causing too much or too little activity. These fluctuations in glutamatergic action lead to degradation of nerve and brain tissue. [3]
By keeping glutamatergic pathways under control, Tianeptine inhibits the body's harmful responses to stress. This leads to increased neuroplasticity, which allows the brain to handle anxiety and depression more readily. The benefits of neuroplasticity also extend into the domain of nootropics by having a positive impact on cognition and working memory.[4] Tianeptine's positive effects on neuroplasticity suggest that it may treat one of the root cause of severe depression rather than simply treat its symptoms. This would imply that Tianeptine has lasting effects on depression and cognition, even when it is no longer administered.
It was recently discovered in 2014 that Tianeptine works as a µ-opioid receptor agonist, which is believed to contribute to its anxiolytic properties. This could also be linked to the possible euphoric effects of Tianeptine that some users experience at higher (recreational) doses. Although Tianeptine acts on µ-opioid receptors, it does not have the high addictive potential that is associated with many opioid drugs.[5] That said, it is still a good idea to avoid taking Tianeptine for long periods of time without interruptions and/or at higher doses than those used in clinical practice.
Positive Effects of Tianeptine
Boosting mood and alleviating depression. [6]
Reducing anxiety and vulnerability to panic attacks. [7]
Improving overall brain health as a neuroprotectant.[8]
Enhancing cognition, memory, attention, and reaction time. [9]
Dosage Information
Prescription Tianeptine (Stablon) comes packaged in 12.5 mg tablets, which is considered a single dose. Tianeptine sold by nootropics vendors come in powder form, so doses should be measured out with a milligram scale to ensure accuracy.
Because Tianeptine has a relatively short duration of action (about 3-4 hours), three of these doses are taken throughout the day, waiting 3-4 hours between each dose. Tianeptine is administered orally, and there is no evidence that would warrant any other route of administration.
Recently some nootropic vendors have started selling tianeptine sulfate, which, according to them, is longer lasting compared to the regular sodium salt. There doesn't seem to be any scientific evidence for this statement, however.
Side Effects, Tolerance, and Toxicity
Tianeptine has a similar side effect profile to more traditional antidepressants but does not cause the sexual dysfunction associated with SSRIs. It also does not exhibit anticholinergic effects that are common with TCAs. The most common side effects include nausea, constipation, abdominal pain, headache, and dizziness. However, all of these possible effects only occur in less than 1% of users.
Because Tianeptine is not monoaminergic in its mechanism of action, it is not considered a risk to take it alongside monoaminergic antidepressants. However, it should not be taken with MAOIs to avoid the risk of hypertension and seizures.
Tianeptine is considered safe to take indefinitely, although tolerance can develop over an extended period of use. If you find it necessary to take higher and higher doses to achieve any positive effects, it would be wise to taper off of the substance and take a tolerance break if you still want to use Tianeptine.
Although discontinuation symptoms of Tianeptine are not nearly as severe as with SSRIs and TCAs, it is still not recommended to suddenly stop usage. In addition, Tianeptine can be cycled with other antidepressant nootropics (like selegiline, NSI-189, or moclobemide) to stop tolerance from developing.
The LD50 of Tianeptine is estimated to be 980 mg/kg, so there is a very low chance of consuming a lethal or harmful dose on accident.
Tianeptine stands out among other antidepressants because of its novel modes of action. Rather than temporarily modifying a monoamine imbalance, it aids the brain in healing itself by increasing neuroplasticity.
It is unfortunate that its use has mostly been ignored by the American medical community, but its unscheduled status has opened up opportunities for nootropic usage. Because of its effects on mood, cognition, stress, and neuroplasticity, Tianeptine should definitely be considered by serious users of nootropics.
I highly recommend Tianeptine to anyone who's looking for an antidepressant that does not impair cognition.
1. ↑ Tianeptine: A Novel Atypical Antidepressant that May Provide New Insights into the Biomolecular Basis of Depression (2006)
2. ↑ The monoamine neurotransmitter disorders: an expanding range of neurological syndromes. (2007)
3. ↑ Stress, glucocorticoids and glutamate release: effects of antidepressant drugs. (2011)
4. ↑ The neurobiological properties of Tianeptine (Stablon): from monoamine hypothesis tfo glutamatergic modulation (2010)
5. ↑ The atypical antidepressant and neurorestorative agent Tianeptine is a μ-opioid receptor agonist (2014)
6. ↑ Value of Tianeptine in treating major recurrent unipolar depression. Study versus placebo for 16 1/2 months of treatment (1997)
7. ↑ The effects of Tianeptine or paroxetine on 35% CO2 provoked panic in panic disorder (2004)
8. ↑ Neuroprotective properties of Tianeptine: interactions with cytokines. (2003)
9. ↑ Effect of Tianeptine on cognitive functions in patients with depressive disorders during a 3-month observation. (2011)
Tags antidepressant, anxiolytics, depression, glutamate, neurogenesis, nootropics
Cognitive Health Memantine Nootropics Recovery
Can Nootropics Help With Drug Abuse and Addiction?
Post author By jay
2 Comments on Can Nootropics Help With Drug Abuse and Addiction?
In recent years, evidence has compiled suggesting a common pathologic mechanism underlying addictive behaviours of several substances. Dysregulation of glutamatergic neurotransmission within the prefrontal cortex (PFC) and nucleus accumbens (NA) appears to predispose to a higher tendency towards drug-seeking behaviour.
Thus far, this mechanism has been associated with the addiction potential of cocaine, heroin, nicotine, cannabis, & alcohol, with possible implications for other substances and even non-drug-related compulsive habits such as pathological gambling. Discovery of this shared pathology has led to the investigation of the potential application of existing agents, such as Memantine and n-acetylcysteine.
Could nootropics targeting elements in this key glutamatergic circuit reduce symptoms and complications of substance use disorders?
Glutamate Spillover
«Glutamate spillover» refers to the pathologic cascade in brain chemistry that occurs with chronic abuse of certain substances that results in reinforcement of the behaviour[1].
Prolonged exposure to substances of abuse leads to several maladaptive changes in the glutamatergic PFC-NA pathway, specifically:
Downregulation of glial glutamate transporter-1 (GLT1) expression in the nucleus accumbens. By removing glutamate from the extrasynaptic space, GLT1 prevents inappropriate excitatory stimulation due to an accumulation of the excitatory neurotransmitter.
Decreased ability of presynaptic metabotropic glutamate receptor 2 (mGluR2) to inhibit glutamate release. In normal physiology, mGluR2 autoreceptors manage a feedback loop where increased extracellular glutamate levels trigger a reduction in the presynaptic release of glutamate. This auto-regulatory mechanism also serves to prevent an extracellular accumulation of glutamate.
When glutamate spillover within the non-synaptic extracellular space does occur as a result of the combination of these processes, the following sequelae are may manifest:
Stimulation of postsynaptic mGluR5, AMPA and NMDA receptors.
Upregulation of AMPA and NMDA receptors (increased synaptic plasticity).
Stimulation of extrasynaptic glutamate receptors may also occur.
Increased excitatory tone due to these two processes culminates in impaired inhibition with regard to drug-seeking behaviour as well as increased risk of relapse. Furthermore, persistently elevated glutamatergic tone may lead to neurotoxicity secondary to excessive Ca2+ ion influx. This pathology has also been associated in neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's disease.
n-acetylcysteine (NAC) is a cysteine precursor that has a long history of use for indications ranging from bronchopulmonary disorders to paracetamol overdose. It produces many beneficial effects through a variety of mechanisms ranging from supporting antioxidant processes to suppressing over-reactive immune responses to inhibiting apoptosis. NAC's glutamatergic modulation, however, is of key interest in managing substance use disorders[2].
NAC is converted to L-cysteine in vivo, which enhances the activity of the cysteine/glutamate exchange transporter positioned near the pre-synaptic terminal. This increases the concentration of extracellular glutamate, resulting in increased tonic activation of pre-synaptic mGluR2 autoreceptors. This causes a subsequent decrease in glutamate release. NAC also increases expression of GLT1 and the cysteine/glutamate exchange transporter, promoting the removal of glutamate from the extrasynaptic space and ‹putting it back› in the pre-synaptic area. These effects in concert have been shown to mitigate the complications from glutamate spillover, & have been tested in several small trials with promising results.
When administered in patients with a history of cocaine addiction, NAC was shown to decrease self-reported cocaine use within the 28 days of treatment (mean 8.1 days out of 28 days before treatment & 1.1 days during treatment, p = 0.001)[3], desire to use cocaine (F = 5.07; df = 1,13; p = 0.05), & response to cocaine cues (F = 4.79, df = 1,13, p = 0.05)[4]. A magnetic resonance spectroscopy study confirmed elevated glutamate levels in the dorsal anterior cingulate cortex of cocaine users when compared against non-users (t(7) = 3.08, p = 0.02), and also showed a reduction 1 hour after a single 2.4 g dose of NAC[5].
With regard to cannabis, 2.4 g/day NAC decreased craving in one 4-week open label study of 24 patients[6]; in a double-blind placebo-controlled trial, subjects given 2.4 g/day NAC in addition to counselling were 2.4 times more likely to test negative on urinalysis (95%CI 1.1 to 5.2) but there was no difference in number of reported days of cannabis use[7].
The dosage for managing consequences of substance use disorders in trials ranged from 1.2 to 2.4 g by mouth daily. Benefits on neurochemistry may occur with single doses although significant alterations in behaviour may take days to weeks. The pharmacodynamic effect also depends upon the history of substance use and individual predisposition to addictive behaviour.
NAC is significantly protein-bound (80%). It is metabolised in the liver via non-CYP450 pathways. NAC and its metabolites are primarily eliminated in the urine, with a half-life of 5.6 hours in adults[8].
NAC is generally well-tolerated. Nausea, vomiting, rash, and fever have been reported.
Memantine (Namenda®) is an uncompetitive NMDA receptor antagonist most commonly used in the management of moderate-to-severe Alzheimer's disease. In addition to its glutamatergic modulation, memantine also acts as an agonist at the D2 and nicotinic acetylcholinergic receptors (nAChR). Memantine binds and inhibits NMDA receptors with low-to-moderate affinity, most effectively in states of excess glutamatergic activity (such as in substance use disorder). By blocking NMDA receptors, memantine decreases glutamatergic tone[9].
Neurochemical effects of alcohol intoxication in various contexts.
Upregulation of NMDA receptors has been observed with chronic alcohol consumption. Abrupt discontinuation of alcohol removes GABAergic suppression, resulting in the characteristic acute sequelae of alcohol withdrawal (symptoms of excitotoxicity): seizures, hallucinations, tachycardia, and shock. By inhibiting these receptors, memantine may theoretically attenuate symptoms of alcohol withdrawal.
In one RCT of 18 moderate alcohol drinkers (10-30 drinks/week), 30 mg/day memantine significantly decreased alcohol craving before alcohol consumption in comparison to 15 mg/day and placebo[10]. Another placebo-controlled RCT with 10-40 mg/day showed no difference[11].
A subsequent study of 38 patients utilising 20-40 mg/day memantine showed dose-dependent reductions in cue-induced craving[12].
In another RCT of 127 male patients undergoing alcohol withdrawal, administration of 10 mg memantine three times a day decreased apparent withdrawal symptom severity, dysphoria, and need for diazepam[13].
Administration of 60 mg significantly alleviated subjectively-rated symptoms of naloxone-induced opioid withdrawal in 8 heroin-dependent patients[14].
In a study of 67 heroin-dependent subjects, 10-30 mg/day memantine significantly reduced heroin craving, depression, and state & trait anxiety compared to placebo after 3 weeks of use. A separate treatment arm using amitriptyline 75 mg/day achieved similar results but with a higher incidence of side effects and a higher dropout rate[15].
Clinical data on application in cocaine[16],[17] and nicotine abuse[18] is less promising.
The dosage for mitigating substance use disorders in trials ranged from 5 to 60 mg, with 30 mg by mouth once daily showing the best effects for alcohol abuse and 30 to 60 mg by mouth once daily shown to be most effective in limited trials for opioid dependence. Safety is best characterised at doses up to 30 mg, as this dosage is used in Alzheimer's disease. Memantine is typically initiated at 5 mg daily then titrated by 5 mg per week up to the goal dose (30 to 60 mg depending upon the indication).
Memantine undergoes favourable non-hepatic metabolism; its metabolites are minimally active. Individuals with a history of kidney disease should consult a doctor or pharmacist before use, as memantine undergoes significant renal elimination (74% is excreted in the urine). The half-life of memantine ranges from 60-80 hours.
The most common side effects noted at therapeutic doses higher than 7 mg/day are dizziness, headache, confusion, anxiety; increased blood pressure; cough; & constipation[19].
Disrupted regulation of glutamatergic pathways in the prefrontal cortex-nucleus accumbent pathway has been implicated as an underlying pathology among several substance use disorders, including cocaine, alcohol, and opioid dependence.
Therapies such as n-acetylcysteine (NAC) and memantine have demonstrated efficacy in attenuating the symptoms of some of these disorders in small trials.
1. ↑ McClure EA, Gipson CD, Malcolm RJ, Kalivas PW, Gray KM. Potential role of n-acetylcysteine in the management of substance use disorders. CNS Drugs. 2014 02;28(2):95-106.
2. ↑ Brown RM, Kupchik YM, Kalivas PW. The story of glutamate in drug addiction & of n-acetylcysteine as a potential pharmacotherapy. JAMA Psychiatry. 2013 09;70(9):895-7.
3. ↑ Mardikian PN, LaRowe SD, Hedden S, Kalivas PW, Malcolm RJ. An open-label trial of n-acetylcysteine for the treatment of cocaine dependence: a pilot study. Prog Neuropsychopharmacol Biol Psychiatry. 2007;31:389-94.
4. ↑ LaRowe SD, Myrick H, Hedden S, Mardikian P, Saladin M, McRae A, et al. Is cocaine desire reduced by n-acetylcysteine? Am J Psychiatry. 2007;164:1115-7.
5. ↑ Schmaal L, Veltman DJ, Nederveen A,van den Brink W, Goudriaan AE. n-acetylcysteine normalizes glutamate levels in cocaine- dependent patients: a randomized crossover magnetic resonance spectroscopy study. Neuropsychopharmacology. 2012;37:2143-52.
6. ↑ Gray KM, Watson NL, Carpenter MJ, LaRowe SD. n-acetylcysteine (NAC) in young marijuana users: an open-label pilot study. Am J Addict. 2010;19:187-9.
7. ↑ Gray KM, Carpenter MJ, Baker NL, DeSantis SM, Kryway E, Hartwell KJ, et al. A double-blind randomized controlled trial of n-acetylcysteine in cannabis-dependent adolescents. Am J Psychiatry. 2012;169:805-12.
8. ↑ Medscape® 5.1.2, (electronic version). Reuters Health Information, New York, New York.
9. ↑ Zdanys K, Tampi RR. A systematic review of off-label uses of memantine for psychiatric disorders. Prog Neuro-Psychopharmacol Biol Psychiatry. 2008 8/1;32(6):1362-74.
10. ↑ Bisaga A, Evans SM. Acute effects of memantine in combination with alcohol in moderate drinkers. Psychopharmacology 2004;172:16–24.
11. ↑ Evans SM, Levin FR, Brooks DJ, Garawi F. A pilot double-blind treatment trial of memantine for alcohol dependence. Alcoholism: Clin Exp Res 2007;31(5):775–82.
12. ↑ Krupitsky EM, Neznanova O, Masalov D, Burakov AM, Didenko T, Romanova T, et al. Effect of memantine on cue-induced alcohol craving in recovering alcohol-dependent patients. Am J Psychiatry 2007a;164(3):519–23.
13. ↑ Krupitsky EM, Rudenko AA, Burakov AM, Slavina TY, Grinenko AA, Pittman B, et al. Antiglutamatergic strategies for ethanol detoxification: comparison with placebo & diazepam. Alcoholism: Clin Exp Res 2007b;31(4):604–11.
14. ↑ Bisaga A, Comer SD, Ward AS, Popik P, Kleber HD, Fischman MW. The NMDA antagonist memantine attenuates the expression of opioid physical dependence in humans. Psychopharmacology 2001(157):1–10.
15. ↑ Krupitsky EM, Masalov DV, Burakov AM, Didenko TY, Romanova TN, Bespalov AY, et al. A pilot study of memantine effects on protracted withdrawal (syndrome of anhedonia) in heroin addicts. Addict Disord Treat 2002;1(4):143–6.
16. ↑ Collins ED, Vosburg SK, Ward AS, Haney M, Foltin RW. Memantine increases cardiovascular but not behavioral effects of cocaine in methadone-maintained humans. Pharmacol Biochem Behav 2006;83(1):47–55.
17. ↑ Collins ED, Ward AS, McDowell DM, Foltin RW, Fischman MW. The effects of memantine on the subjective, reinforcing, & cardiovascular effects of cocaine in humans. Behav Pharmacol 1998;9(7):587–98.
18. ↑ Thuerauf N, Lunkenheimer J, Lunkenheimer B, Sperling W, Bleich S, Schlabeck M, et al. Memantine fails to facilitate partial cigarette deprivation in smokers—no role of memantine in the treatment of nicotine dependency? J Neural Transm 2007;114:351–7.
19. ↑ Micromedex® 1.0 (Healthcare Series), (electronic version). Truven Health Analytics, Greenwood Village, Colorado, U.S.A. Available at: http://www.micromedexsolutions.com/
Tags abuse, addiction, drug abuse, drugs, glutamate, memantine, N-acetylcysteine, NAC, nootropics, recovery, substance abuse, substance use, substance use disorder
The Neurological Benefits of Sarcosine and D-Serine
No Comments on The Neurological Benefits of Sarcosine and D-Serine
Sarcosine and D-Serine are two endogenous substances that are currently being researched for a number of conditions. Although these substances have many interesting properties and may be effective add-on treatments to disorders such as depression and schizophrenia, they are too nonspecific to work effectively as a standalone, and should never be used in place of a doctor's recommendation. That being said, there is some promising evidence for a nootropic, antidepressant and antipsychotic effect.
D-serine vs L-serine
This article includes references from studies using both enantiomers of serine. The two may have somewhat similar effects since L-serine is converted to D-serine by serine racemase, an enzyme that requires vitamin B6 to function. It is thus important to supplement vitamin B6 when supplementing L-serine.
Studies involving both forms of serine clearly demonstrate its interesting scope of effect. That being said, L-serine may be less effective since it requires an extra step before it can be used by the body.
Mood and Depression
D-serine produces both acute[1] and chronic[2] antidepressant effects in animal models. Chronic use was also reported to lower markers of anxiety. Studies have also shown that it may prevent cognitive impairment in subjects exposed to stressful situations[3] (like a job interview) but not in normal day-to-day situations. D-serine, therefore, does not strictly meet the definition of a nootropic. It is, however, ubiquitous in the body, and with many interesting effects in promoting cerebral health, certainly a worthy supplement.
Sarcosine was the star of a landmark 2013 study, which underpinned a role of the Glycine transporter 1 (GlyT1) in depression[4]. The antidepressant effect of sarcosine and other GlyT1 inhibitors may be related to the increased levels of glycine, an inhibitory neurotransmitter that seems to have an anti-stress effect. The study found sarcosine monotherapy to be superior to the SSRI citalopram (Celexa) in remitting depression, with rapid onset of action and few side-effects.[5] The role of glycine in mental disorder may be much larger than originally thought.
As expected, users have reported varying levels of effectiveness from sarcosine as an antidepressant, with some drawing a comparison between ketamine or citalopram, while others have not noticed a significant effect. The research has suggested a strong general effect, which may still nevertheless depend on the individual.
The glutamate system is the largest excitatory system in the brain and it commands functions across every region, so one would expect sarcosine to be useful in depression, memory loss, or interestingly, psychotic disorders. The glycine transporter's influence over NMDA receptors (which are essential for memory and learning) may also explain why sarcosine makes a useful adjunctive therapy to antipsychotics. It's all to do with the involvement of NMDA and glutamate in schizophrenia:
… the hypofunction hypothesis of glutamatergic neurotransmission via N-methyl-D-aspartate (NMDA) receptors in the pathophysiology of schizophrenia suggests that increasing NMDA receptor function via pharmacological manipulation could provide a new therapeutic strategy for schizophrenia. The glycine modulatory site on NMDA receptor complex is the one of the most attractive therapeutic targets for schizophrenia. […] Some clinical studies have demonstrated that the GlyT-1 inhibitor sarcosine (N-methylglycine) shows antipsychotic activity in patients with schizophrenia. Currently, a number of pharmaceutical companies have been developing novel and selective GlyT-1 inhibitors for the treatment of schizophrenia..
Because of the diverse actions of the glycine transporter and its involvement in other neurotransmitter systems, sarcosine has also been found to modulate striatal dopamine release. This may help further explain its antipsychotic properties.
While it may not be terribly effective on its own, used in conjunction with pharmaceuticals, sarcosine can deliver a real knockout blow[6], conveniently complimenting pharmaceuticals in treating both negative and positive symptoms. This is particularly remarkable because most pharmaceuticals were developed to address only positive symptoms; there has been a race to find more effective treatments for the negative symptoms, which have often come in the form of over-the-counter supplements, exercise programs, and specific diets.
Sarcosine and N-acetylcysteine were both found to restore glutamate activity in mGluR5 knockout mice[7] Low activity of this receptor may be related to schizophrenia. Interestingly, positive allosteric modulators of mGluR5 may have nootropic properties. [8]
Sarcosine is known to have potential in Parkinson's[9] and other dopamine dysfunction disorders, such as ADHD.[10] Sarcosine and its metabolite glycine modulate dopamine in the striatum[11], which includes the hippocampus.
Another study[12] has confirmed as helpful the addition of sarcosine to antipsychotic therapy, concluding it increases survival of neurons and glial cells in the dorsolateral prefrontal cortex (a key structure damaged by aging and drug abuse, it is involved in executive functions, such as working memory, cognitive flexibility, planning, inhibition, and abstract reasoning). Sarcosine may soon become a popular supplement in the psychiatric industry.
Even though they are far from being popular nootropic supplements, D-Serine and Sarcosine are two fascinating compounds.
If you are being medicated for schizophrenia or depression, you should definitely consider supplementing one of these two compounds to augment your psychiatric medication. Sarcosine, in particular, is very inexpensive and has a lot of evidence backing up its use. [13] [14]
Nootropic users who have tried Sarcosine report improvements in focus, motivation[15] and visual acuity[16], and there is some evidence that it may help those living with ADHD.[17]
1. ↑ Acute D-serine treatment produces antidepressant-like effects in rodents. (2012)
2. ↑ Effects of Chronic D-Serine Elevation on Animal Models of Depression and Anxiety-Related Behavior. (2013)
3. ↑ D-serine prevents cognitive deficits induced by acute stress. (2014)
4. ↑ Inhibition of glycine transporter-I as a novel mechanism for the treatment of depression. (2013)
6. ↑ Adding Sarcosine to Antipsychotic Treatment in Patients with Stable Schizophrenia Changes the Concentrations of Neuronal and Glial Metabolites in the Left Dorsolateral Prefrontal Cortex. (2015)
7. ↑ The glutamatergic compounds sarcosine and N-acetylcysteine ameliorate prepulse inhibition deficits in metabotropic glutamate 5 receptor knockout mice. (2010)
8. ↑ mGluR5 positive allosteric modulators facilitate both hippocampal LTP and LTD and enhance spatial learning (2009)
9. ↑ Activation of N-methyl-D-aspartate receptor glycine site temporally ameliorates neuropsychiatric symptoms of Parkinson's disease with dementia. (2014)
10, 17. ↑ Sarcosine treatment for oppositional defiant disorder symptoms of attention deficit hyperactivity disorder children. (2016)
11. ↑ Modulation of striatal dopamine release by glycine transport inhibitors. (2005)
12. ↑ Glycine transporter inhibitor sarcosine changes neuronal and glial parameters in the left dorsolateral prefrontal cortex and glutamatergic parameters in the left hippocampus in stable schizophrenia (2016)
13. ↑ Sarcosine or D-serine add-on treatment for acute exacerbation of schizophrenia: a randomized, double-blind, placebo-controlled study. (2005)
14. ↑ A randomized, double-blind, placebo-controlled comparison study of sarcosine (N-methylglycine) and D-serine add-on treatment for schizophrenia. (2010)
15. ↑ Sarcosine – The Model NMDA-Receptor Co-Agonist – Brain Health – LONGECITY
Tags antidepressants, antipsychotics, D-serine, glutamate, glycine, NMDA receptors, nootropics, Sarcosine


text:
University of East London students pledge to save youngsters' lives
Geoff Thompson MBE talking to students at the University of East London USS Campus. Picture: KEN MEARS
More than 300 students have taken part in a coaching day aimed at saving the lives of young people.
More than 300 students have signed up to be coaches. Picture: KEN MEARS
Youngsters from the University of East London (UEL) have signed up to a social coach leadership programme pioneered by the charity, The Youth Charter.
The chairman of UEL's board of governors, Geoff Thompson, said: "There were 135 people killed in London in 2018, of whom 40 per cent were 15 to 25 year olds. This year there have already been 11 deaths.
"Every life is priceless and I believe that we can effect change."
Under the scheme trained mentors help tackle anti-social behaviour among disaffected young people.
Organisers hope it will keep at-risk youngsters from straying into a life of crime by involving them in activities such as sport, media, culture and the arts.
Five time world karate champion Mr Thompson set up The Youth Charter in Manchester 26-years ago after the shooting of 14-year-old Benji Stanley in Moss Side.
Its message is that sport and the arts can be used to divert disaffected youth from crime by building young people's self-confidence and skills.
Student, Elliott Webb, said: "It was seeing violence and drugs on the streets and friends being killed that made me want to be a social coach and come on this coaching day.
"I want to be able to spin it on its head and turn things round so that instead of knives and violence, we can turn things into a positive."
Fellow student, Joan Eitzenberger, wanted to become a social coach to motivate others.
"I believe that motivation and life purpose is very important. I grew up in different cultural backgrounds and I think I can help others through my own experiences."
The programme targets young people aged 10 to 19 with coaches volunteering two hours a week.
Mr Thompson said that it was never too late to turn away from a life of crime.
"We talk to gang members and, while they think it's too late to change, they may be persuaded to leave younger kids alone."
All 300 students took part in a workshop on coaching.
They also heard a motivational talk from the chief executive of The Commonwealth Games Federation, David Grevemberg, who gave a personal reflection of working with disaffected young people around the world.

redpajama_set_name: RedPajamaCommonCrawl


In an exceptional location in Italy's Piedmont Milky way region, at an altitude of 1,600 metres, this new Club Med Resort has charming chalet architecture. 20 clusters of chalets around the resort centre give pride of place to premium family accommodation.
Rémy Camoin, who also designed the Punta Cana renovation, was in charge of interior design at Club Med Pragelato. He took his inspiration from the great cultural heritage of the Piedmont region, from Pragelato's Olympic experience and, most important of all, from Italian art de vivre: Club Med Pragelato is a modern interpretation of the traditional Italian-style guesthouse.
The Club Med Resort gives you direct access to Pragelato and Via Lattea (Milky Way), which are two different ski domains. But you set off from the same starting point for both domains.
The gondola right at the top of the pizza takes 60 people at a time, is fast and leaves every 10 mins and delivers you to the top of Pragelato. The village is ski in ski out, there is a lovely long winding blue/red run (8.5km) that takes you back to the gondola. The area is vast and links with Montgenevre in France.
A free shuttle takes guests to Pragelato town centre and to Sestrières.
Club Rooms - Elegant and delightful room (25 m² / 270 sq ft) is perfectly equipped to ensure your total well being.
Family Club Apartments (max occupancy 6) - Duplex apartment comprising a ground floor with a lounge area and an upstairs with two bedrooms, separated by a door. The apartments have two shower rooms.
Family Club Accommodation (max occupancy 5) - (46 m²) Charming accommodation comprising 2 rooms on two levels: the parents' room with door, upstairs, and the children's room with a sliding door, on the ground floor.
Deluxe Rooms - A spacious room combining comfort and luxury with a lounge area. You'll fall for the charm of its true mountain spirit.
Suites - A 64 m² Suite (688 sq ft) with whirlpool bath, 2 bedrooms and lounge: all the comfort you could wish for after a great day's skiing.
Please note that as the Village is made up of small chalets, there is never more than one of each room type in a chalet – IE two Club Rooms will be in two different chalets. Families are advised to book family suites so that they can be together.
Ll Piemonte - Il Piemonte is just the place to come after a good day out on the slopes. With traditional Italian mountain cuisine, tasteful décor and stunning views of the mountains, what more could you possibly want? Make sure you try some of the local specialities while you're here! With the buffet, you can choose exactly what you want, so it's completely up to you. Go ahead!
La Tana - La Tana provides you with the genuine Italian dining experience. You'll find mountain speciality dishes such as fondue and pierrade, and as well as serving Italian wines, the restaurant sometimes organises wine-tasting sessions. Our friendly and helpful staff are on hand to help you make the best choice.
La Trattoria - La Trattoria is one of the Resort's great places to wine and dine. Enjoy a pizza, salad or pasta for lunch or dinner, with live music to create an unforgettable atmosphere. For evening meals, you'll need to book at Reception.
The Chalet Mollino - You'll find the Chalet Mollino at 2,300 metres (7,545 ft), which makes it perfect for lunch after a good morning's skiing. Traditional mountain architecture is combined with a contemporary spirit, making this the ideal setting for the 21st century skier. The mountain specialities and friendly staff create an atmosphere that will bring you back again and again!
The Lanterna - La Lanterna provides great atmosphere and festive moments. The bar's comfy seating areas, great views and elegant decor make it an ideal place to spend time with friends and loved ones, and it's open all day long.
The Dolce Vita - Le Dolce Vita lives up to its name! An exclusive lounge bar on the 2nd floor of the Resort, this is a cosy and intimate space with a friendly atmosphere and upscale decor.
Drinks are available all day and evening (during bar opening hours) in all the bars in the Resort.


text:
Title: Interpreting Gödel : historical and philosophical perspectives
Author: Chen, Long
Awarding Body: King's College London
Current Institution: King's College London (University of London)
The main project of the thesis is to provide a comprehensive examination of Gödel's philosophy of mathematics and logic, in defence of his Platonism and the idea of mathematical intuition. The whole work is considered to be partly historical, explaining Gödel's ideas and arguments in comparison with his contemporaries such as Carnap, Russell, Turing and Hilbert; partly mathematical, relying especially on his incompleteness theorem to refute certain philosophical positions; and partly philosophical, shedding light on debates in current discussions of philosophy of mathematics and logic such as the nature of paradoxes, the indispensability argument, the feasibility of formalism, etc. After the introduction, chapter one deals with Gödel's critique and refutation of Carnap's syntactical view of mathematics, which interprets mathematics purely in terms of linguistic rules of symbols, and thus void of content. Chapter two discusses Gödel's criticism of Russell's constructivistic view towards logic, especially his no-class theory and the vicious circle principle. Chapter three turns attention to Gödel's role in the development of computability theory, using it as a case study for conceptual analysis and tries to reconcile the apparent conflict concerning Gödel's remarks on Turing, who gave a "precise and adequate definition" of mechanical computability and yet committed "a philosophical error" in his argument. The last chapter focuses on Gödel's relation to Hilbert, especially the relation of his incompleteness theorems for Hilbert's finitary consistency proof program and the significance of Gödel's serious engagement with finitism. The thread uniting all the discussions in the chapters is the idea of the incompletability or inexhaustibility of mathematics by pure formalism and the indispensability of abstract concepts and a kind of mathematical intuition in providing a satisfactory foundation for mathematics and in enabling the human mind to surpass any particular mechanism, which Gödel himself considered to be the major philosophical conclusion to be drawn from his logical results.
Supervisor: Beaney, Michael Anthony ; Galloway, David Watson Sponsor: Not available


text:
in: Characters, Demons, Evil Horde,
This article is about the original character. You may be looking for Hordak from She-Ra and the Princesses of Power series.
Ruthless leader of The Evil Horde
Hec-Tor Kur
Dark warlord
Horde World
Present/Great Wars
Leader of vast army
Master of advanced sorcery
Able to reshape body into any machinery
size shifting
Colin Murdock
Keston John
German dubs:
Uli Krohm
Hebrew dubs:
Guy Rushiniak
Hordak is a fictional character in the Masters of the Universe franchise. He is the leader of the Evil Horde, an army of savage warriors, most of whom wear a red bat symbol on their chests to convey their allegiance. He is the former mentor of Skeletor, one of the franchise's main villains. According to most story media, Skeletor betrayed Hordak and trapped him in another dimension before beginning his own conquest of the planet Eternia. Hordak then returned with a vengeance to take over Eternia for himself.
Hordak is recognizable by his grotesque white (sometimes cream/bone colored) face, with sharp red eyes, his flat snout-like nose, red vampire-like fangs and pointed bat-like ears. He wears a collar of bones and black armor over his chest, emblazoned with the Horde bat symbol.[1] His appearance resembles a vampire or bat-like creature, although in some media he appears more cyborg-like.
Hordak is generally recognized as being the lead villain of the She-Ra: Princess of Power cartoon, in which he is the arch nemesis of She-Ra, He-Man's twin sister. In this series, he rules the planet of Etheria with an army of Horde Troopers.
1.1 Minicomics (1985 - 1987)
1.2 Filmation animated series (1985 - 1986)
1.3 She-Ra: Princess of Power
1.4 He-Man and the Masters of the Universe (2002)
1.5 Masters of the Universe Classics (2008)
1.6 She-Ra and the Princesses of Power (2018 - 2020)
1.7 Masters of the Universe Revelation (2021)
1.8 Hordak in other media
3 Behind the Scenes
4.1 Masters of the Universe minicomics
4.2 Princess of Power minicomics
4.3 Golden Books Hardcover
4.4 She-Ra: Princess of Power (cartoon)
Minicomics (1985 - 1987)
Hordak returned from the dimension in which he was imprisoned to wreak vengeance on Skeletor, his old student, while also making his own attempts to destroy He-Man and seize Castle Grayskull. [2]
He was a sorcerer who had since turned his attention to science, and used a combination of magic and technology in his attempts to conquer Eternia (though he favoured the latter). Hordak was involved in many key events in Eternia's past such as the building of the central tower in The Three Towers of Eternia. When he entered the central tower years later, a buzz-saw weapon formed in his chest which could burst forth and cause untold damage to his enemies. [3]
Filmation animated series (1985 - 1986)
Hordak, with Shadow Weaver
She-Ra: Princess of Power
Hordak was the primary antagonist in She-Ra: Princess of Power, in which he rules a Horde occupied Etheria from his fortress in the Fright Zone. Hordak preferred to use technology rather than magic, and had the ability to transform his body into a variety of weapons. He was opposed in his rule of Etheria by the Great Rebellion.
Many years ago, on Eternia, Hordak and his favorite student, Skeletor, kidnapped Adora when she was an infant, but Skeletor was captured and told Man-At-Arms where to find Hordak. Hordak was able to get away to Etheria with the baby Adora, and he saw to it that she grew up to be a Force Captain in the Horde, thanks in part to the spells Shadow Weaver cast on Adora to make her docile. [4]
Hordak answers to the supreme ruler of the Horde, Horde Prime, who was implied to be his own brother.[5]
In the 2002 He-Man and the Masters of the Universe series, Hordak was a Dark warlord from ancient Eternia, who opposed Castle Grayskull's original ruler, King Grayskull, with a massive army. The conflict ended when Hordak commanded his sorcerers to draw Castle Grayskull into the dimension of Despondos. The spell failed with King Grayskull's intervention, and Hordak and his army were banished to the dark dimension instead. [6]
While trapped in Despondos, Hordak saved Keldor's life after he failed to assassinate the Eternian Elders, and had acid splashed in his face when it was deflected by Captain Randor. Hordak saved Keldor by magically removing the damaged flesh and allowed his bare skull to exist in a magical floating state above his shoulders. Having saved his life on the promise of a later price to be paid, Hordak renamed Keldor as Skeletor. [7]
Hordak in the 2002 He-Man and the Masters of the Universe Series.
Some time later, Hordak called upon Skeletor to free him from Despondos, and Skeletor initially seemed powerless to resist his mentor. However, Skeletor surprised the onlooking Evil-Lyn and He-Man by defiantly destroying Hordak's Sanctuary, and thus hoped to seal his former master away forever.
Soon after, Evil-Lyn attempted to free Hordak through different means with the help of Count Marzo, but after He-Man destroyed the Well of Darkness, Marzo absorbed the power of his amulet and fled. [8] It was also revealed that Hordak was responsible for creating that series' Dark Hemisphere on Eternia by performing the Spell of Separation. [9]
According to Ian Richter of Mattel, who initiated most of the storylines on the cartoon, Hordak was going to conquer Eternia in season three and serve as the main villain of the season before finally being overcome by Skeletor. However, the toy line and cartoon series were both canceled after the show's second season, so the third season was never produced. [10]
Masters of the Universe Classics (2008)
Hordak's bio on his card back reads as follows:
Real Name: Hec-Tor Kur™
Second born heir to the Horde Empire, Hec-Tor Kur™ arrived on the planet Eternia® while battling the cosmic warrior He-Ro™. Taking the name Hordak™, he raised an army and challenged the Snake Men™ for rule over the planet. Although he defeated King Hssss™, Grayskull, leader of the free people of Eternia® succeeded in banishing him to the dimension of Despondos™. It was here that centuries later Hordak™ contacted a young alchemist named Keldor™ and began teaching him the ways of the dark arts in exchange for freedom from his extra dimensional prison.[11]
She-Ra and the Princesses of Power (2018 - 2020)
Hordak in She-Ra and the Princesses of Power.
The She-Ra and the Princesses of Power series portrayed Hordak as a clone of his "brother", Horde Prime. Hordak was one of Prime's top Generals, until he was cast out due to a genetic defect and sent on a suicide mission. Instead, Hordak fell through a portal to Etheria, where he quickly set about creating his own empire in an attempt to conquer the entire planet, hoping this act would be enough to convince Horde Prime to take him back into the Horde empire. However, Hordak found that Etheria was cut off from the rest of the universe, and he had no way of contacting Prime.
Over the years, Hordak recruited more followers to his army, and began to experiment with portal technology, hoping to one day summon Prime to Etheria and prove he was not a failure.
Masters of the Universe Revelation (2021)
Main Article: Hordak (Revelation)
Hordak appears in flashback sequences in the Dark Horse Comics comic book series that serves as a prequel to Masters of the Universe: Revelation.
Hordak in other media
While Hordak came to be generally recognized as She-Ra's main adversary, most story media outside of the cartoon focused more on Hordak as one of He-Man's arch enemies. He featured predominantly in the Star and Marvel comic series in the US as an enemy of He-Man, and also in the London Editions comics in the UK.
London Editions also published a short-lived She-Ra comic series, which also featured Hordak as the main villain, explaining that he divides his time between his rulership of Etheria and his attempts at conquering Eternia. The UK comics also state that there are two Fright Zones that he operates from, one on Etheria and one on Eternia, the latter resembling Mattel's Fright Zone playset. The UK comics revealed that he came from the world of Academica, apparently a world dominated by science and industry.
In the Filmation series, Hordak possesses an array of powers. Unlike his treacherous former pupil Skeletor, who relies mostly on magic, the majority of Hordak's powers are seemingly the product of science. He is capable of transforming himself in a variety of ways. For example, he can turn his arm into an energy cannon, which has also been seen emitting fire, become a massive tank, and even transport himself over great distances by becoming a rocket. In the episode "The Sword In The Stone", Hordak even transforms his arm into a vacuum cleaner. Although mechanical in result, these transformations may have been magically instigated, as they occur instantaneously with an eerie glow and sound effect - but we must not forget the Third Clarke's Law: "Any sufficiently advanced technology is indistinguishable from magic"
However, the minicomics and Marvel Star comic books depict Hordak as using magic to a greater extent, more so than science. He is shown to be a powerful dark mage of equal or greater power to Skeletor and most likely has far greater knowledge.
As was the case with Skeletor and He-Man, Hordak received later action-figure iterations that had new special features. As Hurricane Hordak, he has the power to discharge violent whirlwinds via mechanical rotor-blades that replace his right hand. As Buzz-saw Hordak, he can launch a deadly spinning buzz-saw like projectile from his chest. The accompanying minicomics explain the origins of both seemingly technological powers in clearly magical terms.
In the 2002 Mike Young Productions Cartoon, Hordak briefly appeared in flashbacks and in astral form via dimensional portals. Hordak was depicted as a supremely powerful magic-user, seemingly of vastly greater power than Skeletor, and with no apparent reliance on technology whatsoever, other than his Horde Troopers, although it was unknown if those redesigned minions were still intended to be robots like the original versions.
The animation model for Hordak was designed by artists Gerald Forton and Herb Hazelton, based on many different concepts provided by the design department of both Filmation and Mattel.
Masters of the Universe minicomics
Escape from the Slime Pit!
The Warrior Machine!
The Hordes of Hordak
Enter: Buzz-saw Hordak!
Princess of Power minicomics
Golden Books Hardcover
Teela's Secret
She-Ra: Princess of Power (cartoon)
Into Etheria
Beast Island
She-Ra Unchained
Battle for Bright Moon
The Sea Hawk
The Prisoners of Beast Island
The Peril of Whispering Woods
The Laughing Dragon
King Miro's Journey
He Ain't Heavy
A Loss for Words
Horde Prime Takes a Holiday
The Stone in the Sword
The Crown of Knowledge
The Mines of Mondor
Small Problems
The Eldritch Mist
The Price of Freedom
The Reluctant Wizard
Friends Are Where You Find Them
A Talent for Trouble
Gateway to Trouble
The Unicorn King
Into the Dark Dimension
Treasure of the First Ones
Glimmer's Story
Enemy with My Face
Welcome Back, Kowl
The Rock People
Huntara
Micah of Bright Moon
For Want of a Horse
My Friend, My Enemy
Unexpected Ally
Loo-Kee Lends a Hand
Of Shadows and Skulls
Black Snow
Darksmoke and Fire
Magicats
Flowers for Hordak
He-Man and She-Ra: A Christmas Special
Return of the General
A Lesson in Love
The Time Transformer
Above It All
Day of the Flowers
Brigis
The Caregiver
When Whispering Woods Last Bloomed
Romeo and Glimmer
The Perils of Peekablue
The Locket
Shera Makes a Promise
Bow's Magical Gift
Sweet Bee's Home
Glimmer Come Home
Portrait of Doom
Hordak's Power Play
Assault on the Hive
The Bibbet Story
Swifty's Baby
The Price of Deceit
The Power of Grayskull
He-Man.org
Ultimate She-Ra Guide
↑ http://princessofpower.co.uk/pages/images/toys/dolls2000/hordak-box-back.jpg 2000s-era design art
↑ Hordak: The Ruthless Leader's Revenge!
↑ Enter: Buzz-saw Hordak!
↑ The Secret of the Sword
↑ The Peril of Whispering Woods
↑ The Power of Grayskull
↑ The Price of Deceit
↑ History
↑ Separation
↑ He-Man.org Q&A with Ian Ritcher
↑ http://i.toynewsi.com/g/index.php?mode=view&album=Mattel%2FMOTU%2FHordak&pic=03.jpg&dispsize=600&start=0 2009 Hordak action figure biocard


text:
Home/Sociolinguistics/Register in linguistics with types/Some other registers
Register in linguistics with types/Some other registers
Ahmad JavedJanuary 29, 2023
Registration in linguistics
In linguistics, registration is defined as the way a speaker uses language differently in different circumstances. Think about the words you choose, your tone of voice, even your body language. You probably behave very differently when talking to a friend than at a formal dinner or during a job interview. These variations of informality, also called stylistic variation, are known as registers in linguistics. They are determined by factors such as social occasion, context, purpose, and audience. In this article we will provide you information about the register in linguistics.
The registers are marked by a variety of specialized vocabulary and phrase turns, colloquialisms and the use of jargon, and a difference in intonation and rhythm; In "The Study of Language," linguist George Yule describes the function of jargon as helping to "create and maintain connections between those who see themselves as 'internal' in some way and to exclude the 'external'".
The records are used in all forms of communication, including written, spoken, and signed. Depending on the grammar, syntax, and tone, the register can be extremely rigid or very intimate. You don't even need to use a real word to communicate effectively. An exasperated snort during a debate or a smile while signing "hello" says a lot.
Types of Register in Linguistics
Below are types of register in linguistics.
1-Formal
Formal registration is almost always used in written communication, especially in environments professionals. It may be necessary to use it in oral communication as well. It is characterized by its impersonality and absence of emotion.
We must use it in:
Claim letters
Professional letters and emails (depending on context)
Academic articles (according to context)
It is not appropriate, except for specific exceptions, in:
Casual meetings between coworkers
Communication with trusted people
Contractions should not be used in any case.
Set phrases, colloquial expressions, puns, and exaggerations should be avoided.
It is preferable to avoid abbreviations and acronyms. Informal abbreviations should never be used.
Phrases should not be started with words like " like ", " but ", " also ", but with formal connectors like " likewise ", " nevertheless " or " furthermore ".
Sentences should be complete, with as few omissions as possible, and with more length and complexity than in other styles.
2-Neutral
The neutral register is the most common in broadcast media. It is less elaborate than the formal one, but with the impersonality and lack of emotionality that characterize it. It is also sometimes called " semi-formal registration ."
Its main function is to transmit information, so it is ideal for:
Technical texts
Professional communication (depending on context)
In contexts where it is not very clear which register to use, it is preferable to opt for the formal or the neutral one.
It does not contain as many courtesy formulas as the formal record.
It is more direct, with shorter sentences and with less ornamentation.
Informal abbreviations, set phrases, or contractions should not be used.
3-Informal
The informal register, also called colloquial, is the most common in oral expression. It is the one we use with friends, family, casual situations at work, and other lighthearted contexts. If there is any doubt about which registry to use, it is preferable to avoid starting with the informal registry, unless our interlocutor does so.
It is used to convey affection, express emotion, get closer to our interlocutor and communicate in a relaxed way, so it is ideal for:
Personal emails and letters
Mobile messages and chat
Personal blogs and social networks
As it is the freest form of expression, it does not have specific rules or characteristics, but this register contains elements that cannot be found in the others:
Vulgar expressions, puns, set phrases, and exaggerations.
Figurative language.
Symbols, emoticons, abbreviations, and acronyms.
Incomplete sentences (for example, with ellipsis).
Absence of structuring by paragraphs.
Shorter and less elaborate sentences.
Less rigorous punctuation (additional exclamation and question marks).
1-Frozen
This form is sometimes called a static record because it refers to historical language or communication that is intended to remain unchanged, such as a constitution or sentence. Examples: The Bible, the Constitution of the United States, the Bhagavad Gita, "Romeo and Juliet".
2-Consultative
People often use this record in conversations when speaking with someone who has specialist knowledge or offering advice. The tone is usually respectful (use of courtesy titles), but can be more informal if the relationship is long-lasting or friendly (a family doctor). Sometimes jargon is used, people can pause or interrupt each other. Examples: local television news broadcast, annual physical exam, service provider such as plumber.
3-Intimate
Linguists say this record is reserved for special occasions, usually between just two people, and often in private. Intimate language can be something as simple as a private joke between two college friends or a word whispered in a lover's ear.
We hope that you have understood the concept of register in linguistics.
Difference between Village and City with definitions
What is Sapir Whorf hypothesis Two versions of theory
Types of Social status
Varieties of language in linguistics on different levels
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text:
package deb

import (
	"archive/tar"
	"io/ioutil"
	"strings"
	"testing"
)

func TestExtractPackageName(t *testing.T) {
	want := "golang-mode"
	got := NewPackage("fixtures/golang-mode_1.1.2-2_all.deb").Name
	if want != got {
		t.Errorf("want = '%v' got = '%v'", want, got)
	}
}

func TestExtractPackageArch(t *testing.T) {
	want := "all"
	got := NewPackage("fixtures/golang-mode_1.1.2-2_all.deb").Arch
	if want != got {
		t.Errorf("want = '%v' got = '%v'", want, got)
	}
}

func TestExtractPackageVersion(t *testing.T) {
	want := "1.1.2-2"
	got := NewPackage("fixtures/golang-mode_1.1.2-2_all.deb").Version
	if want != got {
		t.Errorf("want = '%v' got = '%v'", want, got)
	}
}

func TestGetArchive(t *testing.T) {
	filename := "fixtures/golang-mode_1.1.2-2_all.deb"

	// this variable is just used for type checking
	var archive *tar.Reader
	archive, err := NewPackage(filename).archiveOpen()
	if err != nil {
		t.Fatal("Cannot load fixture", filename, "reason", err)
		return
	}

	_ = archive
}

func TestExtractPackageSource(t *testing.T) {
	want := "golang"
	got, err := NewPackage("fixtures/golang-mode_1.1.2-2_all.deb").Source()
	if err != nil {
		t.Errorf("got error '%v'", err)
	}
	if want != got {
		t.Errorf("want = '%v' got = '%v'", want, got)
	}
}

func TestFindChangelog(t *testing.T) {
	filename := "fixtures/golang-mode_1.1.2-2_all.deb"
	pack := NewPackage(filename)

	clname := "./usr/share/doc/" + pack.Name + "/changelog.Debian.gz"
	r, err := pack.Find(clname)
	if err != nil {
		t.Errorf("Cannot load package changelog %q, reason %q", clname, err)
		return
	}
	defer r.Close()

	b, err := ioutil.ReadAll(r)
	if err != nil {
		t.Error("Cannot load package changelog content, reason", err)
		return
	}
	want := "golang (2:1.1.2-2) unstable; urgency=low"
	got := strings.Split(string(b), "\n")[0]
	if got != want {
		t.Errorf("unexpected changelog content: want '%s', got '%s'", want, got)
	}
}

redpajama_set_name: RedPajamaGithub


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Not the battle to win it, I don't mean. Just the battle to understand it.
I hope we're going to try again to repeal the Costa Hawkins Act, and when we do, we're going to make it clear that that's what we're doing and what it means. I did a lot of work for Prop 10 and definitely noticed people's misconception that it would "pass rent control," but I didn't realize how widespread it was until I read my FB newsfeed.
Supporters and opponents, I am sorry we didn't get this across to you before, so I'm trying now: Proposition 10 would NOT have instituted rent control. Not for a single property anywhere in the state.
What it would have done was REMOVE the strict limits on rent control that are currently in place and keep towns and cities from making the decisions that work for them.
Rent control is like fire, a powerful tool that can turn destructive if not carefully employed, and Prop 10 was smart about rent control. It would have kept the ban on rent control on new builds, because without that rent control tends to suppress development, but it would have redefined "new" as, well, new. It would have guaranteed landlords a reasonable rate of return, so that people who wanted to be decent landlords wouldn't just quit the rental business altogether.
I don't know if these misunderstandings are why it didn't pass, but I have a guess. Only a minority of the state wanted statewide rent control. But I am pretty sure a much higher number would have been willing to have city-by-city rent control, instead of the statewide restrictions on local decisionmaking that we currently have.
File under: Reasons why ballot propositions are a bad way to make laws.
When I explained Prop 10 to people I emphasized that it would return local control so each city could choose rent control or not.
An additional reason for Prop 10 not passing is the huge amount of money behind it from the CA Apartment Assoc. The CAA has been trying to get Mountain View's modest rent control law effectively repealed by amending it to death. They couldn't get enough signatures in time for 2018, but now have enough to go on the ballot for 2020. The MV Tenants Coalition was successful in exposing the lie that the new measure would "improve" rent control.


text:
CPD Courses & Events
CPD/Service Provider Site
CPD & Learning
Understanding Organ and Tissue Donation - The GIVE Trigger
Location : Online
For those Australians facing chronic illness, disability and death, organ and tissue donation is a well-established means of effective treatment. Yet despite recent advances and reforms that have resulted in strong growth in donation rates, the demand for donors continues to exceed availability (Organ and Tissue Authority 2014, p. 5).
Australia's Potential Organ Donor Population
(Organ and Tissue Authority 2015)
Transplantable organs can be the heart, lungs, kidneys, liver, pancreas and intestine, and possible donation tissues include heart valves and other heart tissue, musculoskeletal tissue, skin and parts of the eye (Organ and Tissue Authority 2016). Nurses have the power and responsibility to be an advocate for their patients and their loved ones, as well as future donor recipients, by knowing when to refer any potential donors on to relevant teams.
The way in which a person dies influences which organs and tissues are available for donation and the way the donation process occurs (Organ and Tissue Authority 2016). Before donation can take place, death must be determined in one of two ways: brain death or cardiac death.
All deceased persons can be referred as potential tissue donors. Subject to medical suitability assessment and relevant donor checks, the process may or may not go ahead. Most tissue retrieval can take place up to twenty four hours after death, and age limits range from sixty years for heart tissue, to ninety nine years for eye tissue (Curtis & Ramsden 2012).
Donation After Brain Death
When there is severe brain injury, an increase in the intracranial pressure causes inadequate perfusion pressure of the brain. This creates a cycle of marked cerebral ischaemia and oedema, which in turn further elevates intracranial pressure (Australia and New Zealand Intensive Care Society [ANZICS] 2010). Once intracranial pressure exceeds systemic blood pressure, and therefore ceasing intracranial blood flow, death of the whole brain and brain stem occurs (ANZICS 2010). Severe head injury, stroke or haemorrhage, tumours or infection are all causes of brain death.
The Australian and New Zealand Intensive Care Society (2010), states that determination of brain death must be conducted by two senior doctors, performing the same set of tests to see if the patient has any of the following:
Response to painful stimuli
Brain stem reflexes (pupillary response to light, blinking response when the cornea is touched, eye movement when cold water is instilled in the ear canal)
Cough or gag reflex when the back of the throat is stimulated
Ability to spontaneously breathe when disconnected from the ventilator
In certain circumstances where clinical testing of brain death cannot occur, such as facial trauma or the presence of sedative drugs, then a CT angiogram or perfusion scan are conducted to check for blood flow to the brain (Curtis & Ramsden 2012).
Once brain death has been determined, and if organ donation is to go ahead, the patient is then transferred to the operating theatre where the organ and tissue retrieval surgery will take place. The ventilator is removed during the operation and the patients' heart will stop beating (Organ and Tissue Authority 2016).
Donation After Cardiac Death
The signs of cardiac death or cessation of circulation and absence of life are well known and commonly seen in medicine. It can occur suddenly or after a long illness, and the patient may not necessarily be brain dead, but has sustained such severe injuries that they cannot breathe on their own (ANZICS 2010). Once it is clear that ongoing treatment while the patient is on the ventilator will be unsuccessful, and if organ donation is to be attempted, the patient is moved to the operating theatre where the ventilator is turned off. Organ donation can only go ahead if death is determined within ninety minutes of turning off the ventilator, as the organ will begin to deteriorate after this time due to lack of oxygenation (ANZICS 2010).
Cardiac death is determined when all of the following have occurred:
Immobility
Apnoea
Skin perfusion has ceased
Absence of circulation for a minimum of two minutes (measured by feeling for a pulse or monitoring intra-arterial pressure)
(ANZICS 2010)
GIVE Trigger
The early identification and referral of potential organ and tissue donors can be initiated in most cases in the emergency department, through the use of the GIVE clinical trigger. It denotes part of the systematic approach to organ and tissue donation and asks staff to contact their applicable donation team, whether it be a hospital-based liaison or state donation agency, when no further treatment options are appropriate or available, and the patient meets the trigger criteria.
G – a GCS of five or less
I – intubated
V – ventilated
E – end of life care
(Curtis & Ramsden 2012)
The end of life discussion with family members or guardians may or may not have been conducted at this stage, however this does not mean referral cannot be made, and in some cases the donation team may be the most appropriate people to approach the possibility of organ donation with those involved in the decision.
With Australia's aging population and the incidence of chronic disease on the rise, further improvements in donation rates and transplantation outcomes need to be made in order to meet the current and future needs of those requiring organ and tissue donation. Nurses are often the ones directly involved in patient care, and the main contact for patients' families and loved ones. As already mentioned, this enables us to be able to foresee and refer any potential donors in a sensitive manner, allowing for an informed, dignified and respectful decision making process.
[show_more more="Show References" less="Hide References" align="center" color="#808080″]
Australian and New Zealand Intensive Care Society 2010, The ANZICS Statement on Death and Organ Donation, 3rd edn, Melbourne, VIC, Australia.
Australian Government Organ and Tissue Authority 2014, Organ and Tissue Donation for Transplantation in Australia 2014-2018 Strategic Plan, OTA, Canberra, ACT, Australia, viewed 11 July 2016, http://www.donatelife.gov.au…Plan.pdf
Australian Government Organ and Tissue Authority 2015, Organ and Tissue Donation for Transplantation in Australia 2015-2019 Strategic Plan, OTA, Canberra, ACT, Australia, viewed 17 July 2016, http://www.donatelife.gov.au/s…Plan.pdf
Australian Government Organ and Tissue Authority 2016, Understanding the Donation Process, OTA, Canberra, ACT, Australia, viewed 13 July 2016, http://www.donatelife.gov.au/understanding-donation-process
Curtis, K & Ramsden, C 2011, Emergency and Trauma Care for Nurses and Paramedics, Elsevier Australia, Chatswood, NSW, Australia.
Author Natalie Burke
Natalie is a Critical Care Registered Nurse who started off her nursing career in a rural setting before migrating back to Melbourne where she now works in a busy Emergency Department. Natalie comes from a science background, holding a Bachelor of Science (BSc) with majors in anatomy and physiology, before deciding to change career paths into nursing. She undertook a Master of Nursing Practice (MNP) and has never looked back, going on to complete her Graduate Certificate in Emergency Nursing and developing a keen interest for trauma assessment and management. See Educator Profile
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Social identities predict pro-environmental behavior, but the strength may depend on whether the behavior is visible to others. When an environmentalist considers a pro-environmental behavior such as carrying reusable grocery bags, being observed by others may motivate signaling the valued group membership and may increase behavior ("green to be seen"). When an anti-environmentalist considers a pro-environmental behavior that signals an unwanted social identity, being observed may lead to less behavior ("brown to keep down"). United States residents completed three correlational surveys (total N = 1126) of identity, visibility, and self-reported behavior frequency using the Recurring Pro-environmental Behavior Scale. Three multilevel studies revealed that environmentalist identity predicted pro-environmental behavior more strongly for high-visibility behaviors, controlling for confounds at the person level (attitudes, political identity) and the behavior level (difficulty, effectiveness). This research helps uncover the key social identities and contextual factors that lead individuals to embrace or reject pro-environmental behaviors.
Brick, C; Kim, H.S.; Sherman, D.K (2017). "Green to be seen" and "brown to keep down": Visibility moderates the effect of identity on pro-environmental behavior Journal of Environmental Psychology 51, 226–238.


text:
Q: Tagging documents in SharePoint Can we tag individual SharePoint documents? If so, how can we read the tags of a document using SharePoint object model?

A: Create a managed metadata column for your library and then you can be able to tag individual documents.

redpajama_set_name: RedPajamaStackExchange


Today is the big day for 10xJOY because it's the first release of my 10 handmade items! If you are just hearing about this for the first time, I am making 10 items of one product for the last 10 months of the year and donating 10 percent to charity!
Drum roll….March brings you a bushel (well, 10) of apple baby shoes for those sweet little feet!
My little bear is modeling these delicious little soft soled shoes that will keep little feet stylish, warm, and comfy. The shoes are made using an apple fabric that I designed and printed on a 40% recycled eco-canvas and are lined with a super soft red minky fabric. The soles are made of a white utility fabric that has little grippy dots for slip resistance. They are hand sewn by me and really 10 of a kind.
I'm only selling 10 pairs of this shoe design ever, so get your unique little pair in my etsy shop before they are gone. Three sizes are available.
Here's more exciting news: I'm hosting an instagram giveaway today (I'm having some technical problems with Instagram so I'm going to postpone the Giveaway to Monday) for a cute matching bow headband, so pop on over and enter to win!
A dear friend of mine let me borrow her adorable daughter to model this headband for me. Isn't she such a doll?
Credit: I made these shoes from a pattern designed by Weepereas and the cute bear shirt is from Oh Little Rabbit on Etsy.


We are in the process of growing our offerings to Veterans and First Responders, especially in Gentle Restorative Yoga classes. We deeply appreciate the contributions our public servants make to our community. We also know that such service doesn't come without a price, and we are passionate about trying to help. That is why we are on a mission to offer sanctuary and healing.
We presently are offering Restorative Yoga on Sunday late-afternoons (check the calendar for the latest updates). Veterans and First Responders receive a discount off all regular-priced class passes and memberships. We also offer a variety of Personal Training options; please call or email us to discuss schedules and instructor availability.


What is it about dividend-paying companies that makes them so attractive to the long-term and retired investor? To begin with, dividends act as a beacon that lets investors and retirees know that a company's business model is so fundamentally sound today that it can afford to share a percentage of profits with its shareholders. Secondly, dividends help ease the pain during stock market corrections and bear markets. They don't erase the red arrows, but they certainly help hedge your losses a bit. Finally, and most importantly, dividends can be reinvested back into more shares of stock, allowing your position and future dividends to compound. This last point is where substantial wealth can be created over time.
Let's have a look at which five companies make the cut: The technology sector isn't known for its dividends, but Seagate Technology (NASDAQ:STX) is among the best exceptions. GlaxoSmithKline (NYSE:GSK) hasn't had the easiest go of things over the past couple of years due to the imminent emergence of a generic version of inhaled COPD and asthma blockbuster Advair. Up next, we'll look at a company that's been driving over the competition: General Motors (NYSE:GM). Annaly Capital Management (NYSE:NLY) may take a lot of flak as a mortgage real estate investment trust (mREIT), but it's been among the highest-yielding dividend stocks over the past decade, and it's likely to remain so moving forward. Last, but not least, we have Holly Energy Partners (NYSE:HEP), a midstream oil transportation, terminaling, and storage company, which also happens to be a subsidiary of HollyFrontier.


text:
China Building 62-Mile-Long 'Supercollider' to Produce a Million Higgs Bosons
By Hannah Osborne On 11/14/18 at 2:00 AM EST
Tech & Science LHC China Higgs Boson Dark matter
China is building a particle collider almost four times bigger than the Large Hadron Collider (LHC) and it is expected to produce over one million Higgs boson particles in its first decade of operation.
Plans for the Circular Electron Positron Collider (CEPC)—a 62 mile long collider—were first announced in 2012, a few months after the Higgs boson particle was discovered at the LHC. Now, researchers working on the project have released two new design reports to show what they have been working on over the last six years, and what they are planning to do over the coming decades.
The report shows how the CEPC dwarfs the LHC, which has a circumference of just under 17 miles. It outlines how it can go beyond the LHC's capabilities in terms of the physics experiments that can be carried out—over 10 years, scientists say it will be able to produce one million Higgs bosons, 100 million W bosons and a trillion Z bosons.
Artist impression of what China's collider will look like. IHEP
Like the LHC, the CEPC is circular in shape. It will be located in an underground tunnel and consists of a linear accelerator, a damping ring, a booster, transport lines and a collider. It will be a double ring collider, with electron and positron beams circulating in opposite directions in seperate pipes.
The tunnel it sits in could also be used to host a Super proton proton Collider (SppC)—a proposal for which is currently under consideration. This 'supercollider' would reach energies far beyond the LHC—the LHC was designed to have a maximum collision energy of 14 TeV, while the SppC would operate with an energy of 70 TeV.
"The Conceptual Design Report signifies that we have completed the basic design of the accelerator, detector and civil engineering for the whole project," Professor Gao Yuanning, chair of the CEPC Institutional Board, said in a statement. "Our next step will focus on the research and development of key technologies and prototypes for the CEPC."
The design report was announced at a ceremony held by the Institute of High Energy Physics (IHEP) in Beijing.
Geoffrey Taylor of the University of Melbourne, chairman of the International Committee for Future Accelerators (ICFA) and the Asian Committee for Future Accelerators (ACFA), said: "This is a significant milestone along the road to such an important facility for fundamental physics. I have no doubt the international community looks forward to partnering in the development and operation of the CEPC and in the quest to better understand the basic constituents of matter."
Over the next five years, scientists will carry out extensive research, building prototypes of key technical components for the CEPC. The infrastructure for the collider will also be built. Construction of the CEPC is expected to begin in 2022 and it will be completed in 2030.
Should the CEPC prove successful, scientists are hoping the SppC supercollider could be operational at some point in the 2030s. "As an energy frontier machine, the SPPC could discover an entirely new set of particles," the new report says. "Dark matter remains one of the most puzzling issues in particle physics and cosmology. Weakly interacting massive particles (WIMPs) are still the most plausible dark matter candidates." The SppC, the researchers say, could be used to "substantially extend" the search for WIMPs, potentially providing answers to one of the biggest mysteries in the universe.
China Building 62-Mile-Long 'Supercollider' to Produce a Million Higgs Bosons | Tech & Science
LHC Scientists Might Have Found a Strange New Particle
Strange Quarks Shed Light on Universe After Big Bang
Earth Could Be Shrunk by Particle Accelerators


Fancy enough for a night out and comfortable enough for an afternoon in, enjoy the snazzy stylings of this chic top. Wear it with a set of killer heels to pair perfectly with the sassy stiletto lace panels.
The Stiletto Pullover is knit in the round from the bottom up, with separately worked short sleeves and raglan shoulder decreases. The front and back feature identical lace panels.
This pattern includes written instructions and full charts.


text:
U.N.OWENS MUSICAFE
Charlie Lang
When Charlie's father taught 4 year old Charlie how to play the piano he took to it, and by the time he was 7 he had written his own song about Herbie the Lovebug called "Herbie". Throughout his childhood Charlie won many talent shows while continuing to take piano lessons.
At 16, Charlie recorded "Cruisin'" at A&R Recording with the producer Ken Topolsky. It was positively reviewed by Phil Ramone co-founder of A&R.
Charlie attended the Berklee College of Music for two where he majored in Pop Songwriting.
To date, Charlie has written over a thousand and released 4 albums.
He is a vocalist, songwriter, composer, keyboardist, producer, and owner of Lucid Sun Studios in Circleville, New York.
All Rights Reserved 2022. Created in Atlantic Highlands by some guy.
U.N.OWENS Logo created and designed by the talented RYAN TOTH/HIPPOKAMPUS MURALS


The Dormition (Falling Asleep) of the Theotokos is one of the Great Feasts of the Orthodox Church, celebrated on August 15. For those churches using the Julian Calendar, this feast falls on August 28 in the secular calendar. The Feast of the Dormition, which is also sometimes called the Assumption, commemorates the death, resurrection and glorification of Christ's mother. It proclaims that Mary has been "assumed" by God into the heavenly kingdom of Christ in the fullness of her spiritual and bodily existence.
According to Orthodox Tradition, Mary died like all humanity, "falling asleep," so to speak, as the name of the feast indicates. She died as all people die, not "voluntarily" as her Son, but by the necessity of her mortal human nature which is indivisibly bound up with the corruption of this world. The feast was added to the Roman calendar in the seventh century as the Dormitio. In the eighth century, the title was changed to the Assumptio (Assumption).
The Apostles were miraculously summoned to this event, and all were present except Thomas when Mary passed from this life. She was then buried.
Thomas arrived a few days later, and desiring to see her one more time, convinced the others to open her tomb. Upon doing so, the Apostles discovered that her body was no longer present. This event is seen as a firstfruits of the resurrection of the faithful that will occur at the Second Coming of Christ. The event is normally called the Dormition, though there are many Orthodox parishes in English-speaking countries with the name Assumption. In Greek, Dormition is Koimisis—falling asleep in death—from which the word cemetery derives.
The feast is preceded by 14 days of strict fasting, with the exceptions that fish is eaten on the Feast of the Transfiguration (August 6). On weekdays before the feast, either the Great Paraklesis (service of supplication) or the Small Paraklesis is celebrated.
On the eve of the feast, Vespers is served and contains three Old Testament readings that have New Testament meaning. In Genesis 28:10-17, Jacob's Ladder which unites heaven and earth points to the union of God with men which is realized most fully and perfectly in Mary the bearer of God. "How awesome is this place! This is none other than the house of God, and this is the gate of heaven!" In Ezekiel 43:27-44:4, the vision of the temple with the door to the East perpetually closed and filled with the glory of the Lord, symbolizes Mary. And in Proverbs 9:1-11, Mary is also identified with the "house" which the Divine Wisdom has built for herself.
Sometimes Matins is served on the morning of the feast. The Gospel reading is from Luke 1:39-49, 56. It is read on all feasts of the Theotokos and includes the Theotokos' saying: "My soul magnifies the Lord and my spirit rejoices in God my Saviour, for he has regarded the low estate of his handmaiden, for behold, henceforth all generations will call me blessed."
Divine Liturgy is served on the day on the feast. In some churches, it is the custom to bless flowers on this feast before the Liturgy. The epistle reading is from Philippians 2:5-11, and speaks of "Christ Jesus, who, being in the form of God, did not consider it robbery to be equal with God, but made Himself of no reputation, taking the form of a bondservant, and coming in the likeness of men." The gospel reading is taken from Luke 10:38-42 and 11:27-28 together; this reading is also always read on all feasts of the Theotokos. In it, the Lord says, "blessed are those who hear the word of God and keep it!"
She was translated to life by the One who dwelt in her virginal womb.
Dance with joy, O peoples!
Clap your hands with gladness!
Ascending from earth to heaven.
We ceaselessly praise her in song as truly Theotokos.
"Rejoice, O Virgin, pride of Christians!"
The icon of Panagia Ierosolymitissa located inside the Sepulcher of the Theotokos.
The Account of St. John the Theologian of the Falling Asleep of the Holy Mother of God. from Ante-Nicene Fathers, Volume 8.
This page was last edited on July 31, 2018, at 10:25.
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